Dietary polyunsaturated fatty acids, vitamin E and hypoxia/reoxygenation-induced damage to cardiac tissue.
Polyunsaturated fatty acids (PUFA), in the form of marine oils, contain a large proportion of n-3 long chain fatty acids and have been recommended as a dietary supplement for patients with ischaemic heart disease. It has also been suggested that consumption of diets rich in polyunsaturated fatty acids renders tissues more susceptible to free radical-mediated lipid peroxidation, a process which has been implicated in the mechanisms by which tissues may become damaged following hypoxia and subsequent reoxygenation. We have examined the effect of supplementation of diets with oils of different PUFA composition and different vitamin E content on the accumulation of fatty acids by rat hearts in comparison with the effects on tissue lipid peroxidation and the response of the heart to a standardised form of oxidative stress. Groups of Wistar rats were fed a vitamin E supplemented (100 mg alpha-tocopherol acetate/kg) diet containing either 10% corn oil, 10% menhaden oil or 10% lard, or a low vitamin E diet (2.5 mg alpha-tocopherol acetate/kg) containing either 10% corn oil, 10% menhaden oil or 10% lard for 82 +/- 3 days. Diets supplemented with menhaden oil had a dramatic effect on the incorporation of n-3 fatty acids into the cardiac tissue and increased the susceptibility of this tissue to lipid peroxidation in vitro. The effect of these changes on damage to isolated hearts subjected to 60 min hypoxia and reoxygenation was examined using a modified Langendorff system. Nutritional manipulation of the tissue fatty acids and vitamin E content had no influence on the release of creatine kinase activity from rat hearts subjected to hypoxia/reoxygenation. Thus these data do not support the hypothesis that consumption of diets rich in polyunsaturated fatty acids renders tissues more susceptible to free radical damage induced by hypoxia/reoxygenation.
O'Farrell
S
S
Department of Medicine, University of Liverpool, UK.
Jackson
M J
MJ
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D003402:Creatine Kinase / Q000378:metabolism; D004032:Diet; D004042:Dietary Fats, Unsaturated / Q000378:metabolism / Q000494:pharmacology*; D005227:Fatty Acids / Q000378:metabolism*; D015525:Fatty Acids, Omega-3 / Q000378:metabolism / Q000494:pharmacology*; D005260:Female; D005609:Free Radicals / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism* / Q000473:pathology*; D066298:In Vitro Techniques; D015227:Lipid Peroxidation / Q000502:physiology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar; D014810:Vitamin E / Q000494:pharmacology*
D000975:Antioxidants; D004042:Dietary Fats, Unsaturated; D005227:Fatty Acids; D015525:Fatty Acids, Omega-3; D005609:Free Radicals; D014810:Vitamin E; D003402:Creatine Kinase